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Exercise is a very good and dangerous thing. The harms of exercise provide a workload of sports medicine for the young and orthopaedic surgery for the old. But there are also many specific conditions where appropriate doses of this hazardous intervention may help—fibromyalgia, for instance. A Canadian meta-analysis of 6 studies (J Rheumatol 2008;35:1130–44) provides moderate-quality evidence that aerobic-only exercise training to levels recommended by the American College of Sports Medicine has positive effects on global well-being and physical function, and possibly on pain and tender points. In early rheumatoid arthritis, a randomised trial from Sweden (Arthritis Rheum 2008;59:325–31) found that coaching patients to maintain healthy physical activity has benefits above standard rehabilitation, both in muscle strength and perceived health status; but, the investigators add that “the mechanisms remain unclear, as self-reported physical activity at healthy level[s] did not change.” Trials of exercise are certainly fraught with difficulty, but an Australian team must be congratulated on devising a programme of sham exercise to administer to a group of patients after stroke (J Am Geriatr Soc 2008;56:976–85): this worked as well as most of the “real” exercise modalities they used in this small (n = 52) study.
Exercise may also help you to stay off cigarettes, according to a randomised trial from California (Prev Med 2008;47:215−20); on the other hand, achieving moderate-to-vigorous exercise levels may simply be a good measure of willpower. This trial also assessed the effect of continuing bupropion, which unsurprisingly comes quite high in the pecking order of pharmacotherapies for smoking cessation to be found in a recent Canadian meta-analysis (CMAJ 2008;179:135−44); varenicline may be even better, but the effectiveness estimates have a wide spread, expressed in this paper as 95% credible intervals.
The common end stage of cardiac disease, which we call heart failure, is a miserable condition, and many of those who have it express a wish to die. Clinically, it is highly unpredictable, and doctors can be wildly inaccurate in their guesses about prognosis. One bad prognostic feature is anaemia, and the connection between low haemoglobin and mortality in heart failure is explored in a recent systematic review (J Am Coll Cardiol 2008;52:818–27). Oddly, it does not feature in a clinical and biochemical score for mortality prediction in patients with acute dyspnoea recently proposed by a team from Harvard (Heart 2008;94:1032−7), although this score does include B-type natriuretic peptide (BNP). In fact, sequential measurement of BNP (or the circulating level of the amino-terminal of its pro-hormone) has until recently been the most powerful single predictor of death from heart failure. But a recent study of 786 Austrian patients at all stages of heart failure showed that the vasopressin precursor copeptin outperforms even BNP as a prognostic marker (J Am Coll Cardiol 2008;52:266−72). Predicting death from heart failure may need no scoring system but just a blood test or 2.
Because most doctors rush about amidst a welter of competing tasks and clinical data, scoring systems need to be very simple (or built into basic clinical software) in order to stand any chance of being used. A score for predicting type 2 diabetes has recently been devised on the basis of population data from the Norfolk (UK) section of the EPIC study (Fam Pract 2008;25:191−6). Coming from Cambridge, England, rather than its Massachusetts sister, it makes a virtue of simplicity and stratifies participants according to sex, age, prescription of steroids and blood pressure drugs, body mass index, and smoking status. Those in the top quintile were 22 times more likely to develop diabetes than those in the bottom quintile. But there is always a temptation to “improve” on risk scores by adding just one more indicator, such as the ankle–brachial pressure index (ABI or ABPI) to tweak the Framingham Score for cardiovascular risk. A recent meta-analysis in JAMA 2008;300:197−208 supports this, and an Italian study shows that the ABI can be measured by palpation of the foot arteries rather than requiring Doppler ultrasound; there is even a picture of an Italian general practitioner doing it (Fam Pract 2008;25:228−32).
Local corticosteroid injections also belong in the armamentarium of most general practitioners, but do they actually do much good? A randomised trial of triamcinolone for trigger finger (Ann Rheum Dis 2008;67:1262–6) used normal saline injections as the randomised placebo and found that the steroid was definitely better, with improvement for up to 12 months. But in a double-blinded comparison of injected dexamethasone plus lidocaine versus lidocaine alone for lateral elbow pain, there was no significant difference in outcomes (J Hand Surg [Am] 2008;33:909−19).
Holidays to exotic parts may become a rarer luxury as air fares increase and we become more eco-conscious: more reason to avoid ruining them with traveller’s diarrhoea due to enterotoxicogenic Escherichia coli. Effective protection seems to be afforded by a skin patch containing heat-labile E coli toxin. In a trial reported in Lancet 2008;371:2019−25, two applications worked well before travel to Mexico or Guatemala: Montezuma’s revenge reduced to a slightly sore arm.